Post-translational changes in the redox state of cysteine residues can rapidly and reversibly alter protein functions, thereby modulating biological processes. The nematode C. elegans is an ideal model organism for studying cysteine-mediated redox signaling at a network level. Here we present a comprehensive, quantitative, and site-specific profile of the intrinsic reactivity of the cysteinome in wild-type C. elegans. We also describe a global characterization of the C. elegans redoxome in which we measured changes in three major cysteine redox forms after HO treatment. Our data revealed redox-sensitive events in translation, growth signaling, and stress response pathways, and identified redox-regulated cysteines that are important for signaling through the p38 MAP kinase (MAPK) pathway. Our in-depth proteomic dataset provides a molecular basis for understanding redox signaling in vivo, and will serve as a valuable and rich resource for the field of redox biology.
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http://dx.doi.org/10.1038/s41467-021-21686-3 | DOI Listing |
Alzheimers Dement
January 2025
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, USA.
Introduction: Iron-mediated cell death (ferroptosis) is a proposed mechanism of Alzheimer's disease (AD) pathology. While iron is essential for basic biological functions, its reactivity generates oxidants which contribute to cell damage and death.
Methods: To further resolve mechanisms of iron-mediated toxicity in AD, we analyzed post mortem human brain and ApoEFAD mice.
Biochimie
January 2025
Jagiellonian University Medical College, Faculty of Health Sciences, Department of Medical Physiology, Chair of Biomedical Sciences, 12 Michalowskiego st., 33-332 Cracow, Poland.
Obesity treatment requires an individualized approach, emphasizing the need to identify metabolic pathways of diagnostic relevance. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play a crucial role in metabolic disorders, as receptor deficiencies improves insulin sensitivity and reduces obesity-related inflammation. Additionally, hydrogen sulfide (HS) influences lipolysis, adipogenesis, and adipose tissue browning through persulfidation.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Division of Plant Science and Technology, University of Missouri, Columbia, MO 65211, USA.
Cadmium (Cd) is a pervasive heavy metal pollutant released into the environment through industrial activities such as mining, smelting, and agricultural runoff. This study aimed to investigate the molecular and metabolic impacts of Cd exposure on the silk glands of , a species renowned for producing silk with exceptional mechanical properties. Cd accumulation in spider bodies and silk glands was significantly higher in the low- and high-Cd groups compared to controls, with a dose- and time-dependent increase.
View Article and Find Full Text PDFAntioxidants (Basel)
January 2025
Université de Lorraine, INRAE, IAM, F-54000 Nancy, France.
The oxidative modification of specific cysteine residues to persulfides is thought to be the main way by which hydrogen sulfide (HS) exerts its biological and signaling functions. Therefore, protein persulfidation represents an important thiol-switching mechanism as other reversible redox post-translational modifications. Considering their reductase activity but also their connections with proteins that generate HS and its related molecules, the glutaredoxin (GRX) and thioredoxin (TRX)-reducing systems have potential dual roles in both protein persulfidation and depersulfidation.
View Article and Find Full Text PDFRedox Biol
January 2025
Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USA. Electronic address:
Metabolic pathways fuel tumor progression and resistance to stress conditions including chemotherapeutic drugs, such as DNA damage response (DDR) inhibitors. Yet, significant gaps persist in how metabolic pathways confer resistance to DDR inhibition in cancer cells. Here, we employed a metabolism-focused CRISPR knockout screen and identified genetic vulnerabilities to DDR inhibitors.
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